• T Seifert, P Rasmussen, N H Secher, and H B Nielsen.
• Department of Anaesthesia, The Copenhagen Muscle Research Centre, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. tseifert78@gmail.com
• Acta Physiol (Oxf). 2009 Jul 1;196(3):295-302.

AimBeta-blockers reduce exercise capacity by attenuated increase in cardiac output, but it remains unknown whether performance also relates to attenuated cerebral oxygenation.MethodsActing as their own controls, eight healthy subjects performed a continuous incremental cycle test to exhaustion with or without administration of the non-selective beta-blocker propranolol. Changes in cerebral blood flow velocity were measured with transcranial Doppler ultrasound and those in cerebral oxygenation were evaluated using near-infrared spectroscopy and the calculated cerebral mitochondrial oxygen tension derived from arterial to internal jugular venous concentration differences.ResultsArterial lactate and cardiac output increased to 15.3 +/- 4.2 mM and 20.8 +/- 1.5 L min(-1) respectively (mean +/- SD). Frontal lobe oxygenation remained unaffected but the calculated cerebral mitochondrial oxygen tension decreased by 29 +/- 7 mmHg (P < 0.05). Propranolol reduced resting heart rate (58 +/- 6 vs. 69 +/- 8 beats min(-1)) and at exercise exhaustion, cardiac output (16.6 +/- 3.6 L min(-1)) and arterial lactate (9.4 +/- 3.7 mM) were attenuated with a reduction in exercise capacity from 239 +/- 42 to 209 +/- 31 W (all P < 0.05). Propranolol also attenuated the increase in cerebral blood flow velocity and frontal lobe oxygenation (P < 0.05) whereas the cerebral mitochondrial oxygen tension decreased to a similar degree as during control exercise (delta 28 +/- 10 mmHg; P < 0.05).ConclusionPropranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity.

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